全文获取类型
收费全文 | 924篇 |
免费 | 27篇 |
国内免费 | 2篇 |
专业分类
儿科学 | 8篇 |
妇产科学 | 8篇 |
基础医学 | 135篇 |
口腔科学 | 3篇 |
临床医学 | 44篇 |
内科学 | 254篇 |
皮肤病学 | 7篇 |
神经病学 | 61篇 |
特种医学 | 13篇 |
外科学 | 171篇 |
综合类 | 2篇 |
预防医学 | 15篇 |
眼科学 | 8篇 |
药学 | 101篇 |
中国医学 | 1篇 |
肿瘤学 | 122篇 |
出版年
2023年 | 4篇 |
2021年 | 9篇 |
2020年 | 6篇 |
2019年 | 4篇 |
2018年 | 8篇 |
2017年 | 10篇 |
2016年 | 15篇 |
2015年 | 10篇 |
2014年 | 7篇 |
2013年 | 18篇 |
2012年 | 31篇 |
2011年 | 29篇 |
2010年 | 33篇 |
2009年 | 21篇 |
2008年 | 39篇 |
2007年 | 44篇 |
2006年 | 58篇 |
2005年 | 63篇 |
2004年 | 77篇 |
2003年 | 97篇 |
2002年 | 95篇 |
2001年 | 24篇 |
2000年 | 24篇 |
1999年 | 25篇 |
1998年 | 30篇 |
1997年 | 17篇 |
1996年 | 13篇 |
1995年 | 18篇 |
1994年 | 8篇 |
1993年 | 8篇 |
1992年 | 10篇 |
1991年 | 9篇 |
1990年 | 4篇 |
1989年 | 10篇 |
1988年 | 3篇 |
1987年 | 4篇 |
1986年 | 12篇 |
1985年 | 6篇 |
1984年 | 7篇 |
1983年 | 3篇 |
1982年 | 3篇 |
1981年 | 6篇 |
1980年 | 2篇 |
1979年 | 3篇 |
1978年 | 5篇 |
1977年 | 3篇 |
1976年 | 3篇 |
1974年 | 2篇 |
1973年 | 2篇 |
1955年 | 1篇 |
排序方式: 共有953条查询结果,搜索用时 15 毫秒
951.
952.
Koya Odaira Takahiko Yasuda Kentaro Okada Takuya Shimooka Yukino Kojima Mina Noura Shogo Tamura Shingo Kurahashi Eisuke Iwamoto Masashi Sanada Itaru Matsumura Yasushi Miyazaki Tetsuhito Kojima Hitoshi Kiyoi Shinobu Tsuzuki Fumihiko Hayakawa 《Cancer science》2023,114(3):781-792
CEBPA-IGH, a fusion gene of the immunoglobulin heavy-chain locus (IGH) and the CCAAT enhancer-binding protein α (C/EBPα) gene, is recurrently found in B-ALL cases and causes aberrant expression of C/EBPα, a master regulator of granulocyte differentiation, in B cells. Forced expression of C/EBPα in B cells was reported to cause loss of B-cell identity due to the inhibition of Pax5, a master regulator of B-cell differentiation; however, it is not known whether the same mechanism is applicable for B-ALL development by CEBPA-IGH. It is known that a full-length isoform of C/EBPα, p42, promotes myeloid differentiation, whereas its N-terminal truncated isoform, p30, inhibits myeloid differentiation through the inhibition of p42; however, the differential role between p42 and p30 in ALL development has not been clarified. In the present study, we examined the effect of the expression of p42 and p30 in B cells by performing RNA-seq of mRNA from LCL stably transfected with p42 or p30. Unexpectedly, suppression of PAX5 target genes was barely observed. Instead, both isoforms suppressed the target genes of MEF2 family members (MEF2s), other regulators of B-cell differentiation. Similarly, MEF2s target genes rather than PAX5 target genes were suppressed in CEBP-IGH-positive ALL (n = 8) compared with other B-ALL (n = 315). Furthermore, binding of both isoforms to MEF2s target genes and the reduction of surrounding histone acetylation were observed in ChIP-qPCR. Our data suggest that the inhibition of MEF2s by C/EBPα plays a role in the development of CEBPA-IGH-positive ALL and that both isoforms work co-operatively to achieve it. 相似文献
953.
Nobuhisa Morimoto Takayasu Mori Shingo Shioji Hatsumi Watanabe Keigo Sakai Katsuo Mori Ayumi Yamamura Asami Hanioka Yuichiro Akagi Tamami Fujiki Shintaro Mandai Yutaro Mori Fumiaki Ando Koichiro Susa Soichiro Iimori Shotaro Naito Eisei Sohara Shinichi Uchida 《International journal of rheumatic diseases》2023,26(8):1603-1607
Avacopan is a novel C5a receptor antagonist recently approved for the treatment of microscopic polyangiitis and granulomatosis with polyangiitis. To our knowledge, thrombocytopenia induced by avacopan has not been reported. We report a case of a 78-year-old man with microscopic polyangiitis who developed rapidly progressive glomerulonephritis (RPGN) and vasculitis neuropathy. After developing RPGN, he was treated with prednisolone, which was ineffective. As the dosage of corticosteroids was decreased, he developed impaired dorsiflexion of the left ankle, tingling and numbness in his feet, consistent with vasculitis neuropathy. After a 3-day administration of methylprednisolone, we started avacopan and prednisolone 20 mg/d to reduce the corticosteroid dosage. One week after starting avacopan, platelet counts began to decrease, eventually leading to the cessation of the drug. The possibility of thrombotic microangiopathy and heparin-induced thrombocytopenia was considered unlikely given the clinical course and laboratory studies. After 3 weeks of avacopan cessation, platelet counts began to increase, suggesting avacopan as the most probable cause of thrombocytopenia. Our case highlights the importance of postmarketing surveillance of avacopan to identify its adverse events that were not reported in clinical trials to ensure its safe use. Clinicians should carefully monitor platelet counts when using avacopan. 相似文献